Mouse Models of Human Proprotein Convertase Insufficiency.
PCSK
knockout mouse models
precursor processing
proprotein convertase
Journal
Endocrine reviews
ISSN: 1945-7189
Titre abrégé: Endocr Rev
Pays: United States
ID NLM: 8006258
Informations de publication
Date de publication:
25 05 2021
25 05 2021
Historique:
received:
03
09
2020
pubmed:
1
1
2021
medline:
26
4
2022
entrez:
31
12
2020
Statut:
ppublish
Résumé
The kexin-like proprotein convertases perform the initial proteolytic cleavages that ultimately generate a variety of different mature peptide and proteins, ranging from brain neuropeptides to endocrine peptide hormones, to structural proteins, among others. In this review, we present a general introduction to proprotein convertase structure and biochemistry, followed by a comprehensive discussion of each member of the kexin-like subfamily of proprotein convertases. We summarize current knowledge of human proprotein convertase insufficiency syndromes, including genome-wide analyses of convertase polymorphisms, and compare these to convertase null and mutant mouse models. These mouse models have illuminated our understanding of the roles specific convertases play in human disease and have led to the identification of convertase-specific substrates; for example, the identification of procorin as a specific PACE4 substrate in the heart. We also discuss the limitations of mouse null models in interpreting human disease, such as differential precursor cleavage due to species-specific sequence differences, and the challenges presented by functional redundancy among convertases in attempting to assign specific cleavages and/or physiological roles. However, in most cases, knockout mouse models have added substantively both to our knowledge of diseases caused by human proprotein convertase insufficiency and to our appreciation of their normal physiological roles, as clearly seen in the case of the furin, proprotein convertase 1/3, and proprotein convertase 5/6 mouse models. The creation of more sophisticated mouse models with tissue- or temporally-restricted expression of specific convertases will improve our understanding of human proprotein convertase insufficiency and potentially provide support for the emerging concept of therapeutic inhibition of convertases.
Identifiants
pubmed: 33382413
pii: 6056482
doi: 10.1210/endrev/bnaa033
pmc: PMC8152446
doi:
Substances chimiques
Proprotein Convertase 5
EC 3.4.21.-
Proprotein Convertases
EC 3.4.21.-
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
259-294Subventions
Organisme : NIDA NIH HHS
ID : R01 DA042351
Pays : United States
Informations de copyright
© The Author(s) 2020. Published by Oxford University Press on behalf of the Endocrine Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
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